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能够在黑猩猩肝细胞胞质中诱导管状超微结构的非甲非乙型(1型)肝炎病原体:经福尔马林和加热灭活。

Non-A, non-B (type 1) hepatitis agent capable of inducing tubular ultrastructures in the hepatocyte cytoplasm of chimpanzees: inactivation by formalin and heat.

作者信息

Yoshizawa H, Itoh Y, Iwakiri S, Kitajima K, Tanaka A, Tachibana T, Nakamura T, Miyakawa Y, Mayumi M

出版信息

Gastroenterology. 1982 Mar;82(3):502-6.

PMID:6797865
Abstract

We have reported two kinds of viruslike particles derived from human sera that induced morphologically and serologically different types of non-A, non-B hepatitis in chimpanzees. A chimp serum containing one such agent capable of inducing a type of hepatitis with cytoplasmic tubular ultrastructures (non-A, non-B, type 1) was titrated for its infectivity in chimps. Two chimps who received 1 ml of a 10(-2) dilution of the original serum developed the characteristic morphological changes in the liver together with elevated serum transaminase levels, while the other two who received 1 ml of a 10(-4) dilution failed to show such changes. The two who escaped the infection were proven to be susceptible to the agent, because they developed non-A, non-B, type 1 hepatitis when they were challenged by 1 ml of a 10(-1) dilution of the same serum on the 23rd week after the first inoculation. One milliliter of a 10(-1) dilution containing more than 10 chimp infecting units were inactivated in the presence of 1/2000 formalin or by heating at 100 degrees C for 5 min and then given to four other chimps. None of them developed clinical or histologic evidence of non-A, non-B, type 1 hepatitis, thereby indicating that both formalin and heat could destroy the ability of the agent to induce this type of hepatitis.

摘要

我们报道过从人血清中分离出的两种病毒样颗粒,它们可在黑猩猩中诱发形态学和血清学上不同类型的非甲非乙型肝炎。对一份含有能诱发具有细胞质管状超微结构的肝炎(非甲非乙1型)的此类因子的黑猩猩血清,测定其对黑猩猩的感染性。两只接受了1毫升原始血清10⁻²稀释液的黑猩猩,肝脏出现了特征性形态学变化,同时血清转氨酶水平升高,而另外两只接受1毫升10⁻⁴稀释液的黑猩猩未出现此类变化。事实证明,未受感染的那两只黑猩猩对此因子敏感,因为在首次接种后第23周,当它们接受1毫升同一血清10⁻¹稀释液的攻击时,患上了非甲非乙1型肝炎。1毫升含10个以上黑猩猩感染单位的10⁻¹稀释液,在1/2000福尔马林存在下或在100℃加热5分钟后被灭活,然后给另外四只黑猩猩注射。它们均未出现非甲非乙1型肝炎的临床或组织学证据,这表明福尔马林和加热均可破坏该因子诱发此类肝炎的能力。

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